This pathophysiology diagram illustrates the sequential formation of sub-retinal pigment epithelium (RPE) deposits, a key process in the pathogenesis of Age-Related Macular Degeneration (AMD). The five-panel progression depicts the retinal layers from top to bottom: photoreceptor outer segments receiving light, the RPE cell layer (containing a central nucleus and brown melanocytes), and Bruch's membrane above the choriocapillaris. The metabolic mechanism begins with the appearance of micrometer-sized, black cholesterol-containing extracellular lipid droplets beneath the RPE. The sequence then shows the precipitation of magenta-colored hydroxyapatite (HAP) onto these droplets, followed by the recruitment and binding of blue-colored proteins to the HAP surface. The final panel demonstrates a self-driven oligomerization process resulting in a macroscopic yellow sub-RPE deposit (drusen). This educational model highlights the role of lipid accumulation and mineralization in Bruch's membrane aging and the development of early-stage AMD lesions.

A pathophysiology diagram illustrating the signaling pathway through which auranofin and hyperglycemia-induced TXNIP contribute to Retinal Pigment Epithelium (RPE) dysfunction in Diabetic Retinopathy (DR). The flowchart depicts the inhibition of Thioredoxin/Thioredoxin Reductase systems (Trx2/TrxR2 and TrxR1/Trx1) by auranofin and TXNIP. This inhibition triggers Reactive Oxygen Species/Reactive Nitrogen Species (ROS/RNS) stress, leading to mitochondrial dysfunction. Downstream events include mitophagy-lysosome destabilization characterized by the leakage of mitochondrial Damage-Associated Molecular Patterns (Mt-DAMPs) and Cathepsins. This leakage activates the NLRP3 inflammasome, ASC, and Caspase-1, resulting in pro-inflammatory pyroptosis and cellular damage, evidenced by LDH release from ARPE-19 cells. The diagram uses anatomical illustrations of mitochondria, lysosomes, and the NLRP3 inflammasome complex to show cellular organelle involvement. This schematic summarizes the mitochondria-lysosome axis dysfunction and its role in chronic retinal neurodegenerative diseases including Diabetic Retinopathy, Age-related Macular Degeneration (AMD), and Retinitis Pigmentosa (RP).

This composite figure provides a genetic and multimodal imaging analysis of retinitis pigmentosa (RP). Panel (a) is a complex consanguineous pedigree diagram illustrating an inheritance pattern associated with a homozygous RPE65 variant. Filled symbols indicate affected individuals across generations, with a double line indicating consanguinity. Panel (b) is a widefield color fundus photograph of a 42-year-old patient's right eye. It demonstrates characteristic features of retinal degeneration, including prominent retinal pigment epithelium (RPE) granularity and subtle scattered white dots, with notable pigmentation changes across the posterior pole and periphery. Panel (c) is a widefield fundus autofluorescence (FAF) image of the same eye, showing a profound and global lack of autofluorescence. This generalized hypoautofluorescence indicates severe dysfunction or loss of fluorophores in the RPE and photoreceptor layers, a hallmark finding in RPE65-related retinopathies. The combined clinical and genetic data illustrate the diagnostic correlation between inheritance patterns and progressive retinal degeneration.